Synergistic Apoptosis in CHO.K1 Cells Recovered from UV Irradiation

• Main Authors: Hsin-Chieh Lan, 藍心婕
• Other Authors: Yin-Chang Liu
• Format: Others
• Language: zh-TW
• Published: 2000
• Online Access: http://ndltd.ncl.edu.tw/handle/63215899945836244636

碩士 === 國立清華大學 === 生命科學系 === 88 === Cell death following exposure to genotoxin, for example, ultraviolet, can occur via several routes, including mitotic catastrophe, extended or permanent cell cycle arrest, and apoptosis. Previously, the massive cell death induced by colcemid after UV exposed in CHO.K1 cells has been proved. Colcemid, a mitosis inhibitor, caused the synergistic cell death cooperated with UV damage and this effect was incubation time and drug dose dependent. Upon exposure to 0.5 mg/ml of colcemid after UV 26 j/m2 treatment, cell morphology was severely altered, cell volume decrease, and condensation of the chromosome was clearly noticeable. Besides this, the fragmentation of genomic DNA indicated cell death caused by drug and UV was probably due to apoptosis. To determine if other cell cycle inhibitors would promote cell death in the same situation, mimosine, the G1 phase inhibitor were tested and synergistic apoptosis was observed of this drugs also. Different modes of cell death can occur within individual cell type to the genotoxin, so two different cell lines, NIH3T3 and HF-E6, were treated. The results show that there was no obvious diversity between two data of UV exposed alone and coexist with colcemid. The outcomes of HF-E6 cells that lack of p53 protein functions, indicate the synergistic apoptosis might be not due to p53 disruption. Recent work has suggested that cell cycle inhibitors could induce synergistic apoptosis after UV damage dependents on cell type, medicinal dose and incubation time, but not for dysfunction of p53 protein.